Exposure to numerous environmental agents, including lead, mercury, PCBs, and environmental tobacco smoke, has been linked with adverse neurobehavioral effects. Still, the ideal biomarker fof measuring in utero exposure to specific toxicants has not been established and the adverse effects of many potential neurotoxicants have not been rigorously tested. Fetal exposure is typically measured with self-reported surveys, maternal blood and urine, or cord blood. In contrast, meconium as a biomarker is a non-invasive method to simultaneously test for cumulative exposures to numerous toxicants. But it is unclear whether conventional biomarkers or meconium levels are more predictive of the adverse effects linked with specific toxicants. For lead exposure, emerging data indicate that our efforts should emphasize primary prevention, but the efficacy of lead hazard controls are uncertain, especially for children with low blood lead concentrations. The investigators propose to conduct a cohort study of 400 children, followed from less than 16 weeks gestation to 36 months if age, to examine the effect of low-level exposures to prevalent neurotoxicants. Endpoints include behavioral problems, such as conduct disorder and features consistent with ADHD, cognitive deficits, and hearing loss. The investigators will also conduct a nested, randomized controlled trial to test the efficacy of lead hazard controls on the development of adverse neurobehavioral effects. They will test the following hypotheses: 1) Children in the Lead Reduction Group will have blood lead levels that are 2.7 ug/dL (30%) or lower, significantly higher cognitive scores, less hearing loss, and fewer behavioral problems than one Control group at 36 months of age. 2) Fetal and postnatal exposures to pesticides, ETS and lead (at blood levels below 10 ug/dL) are associated with adverse neurobehavioral effects, growth delay and hearing loss in early childhood. 3) Fetal exposures, as measured by survey (ETS), maternal and cord blood (lead, methyl mercury, pesticides and ETS), and urine (pesticides), are less predictive of the adverse effects of toxicants on cognition, behavioral problems and hearing, compared with the same toxicants in meconium. This project, in combination with the research described in Project 2, will test the efficacy of an intervention for the primary prevention of lead toxicity, as measured by lead concentration and neurobehavioral functioning at 36 months of age, serve as a model to evaluate the adverse effects of exposures to multiple prevalent toxicants among fetuses and children test meconium levels as a biomarker of fetal exposure to numerous toxicants, and provide exposure and risk assessment data for residential pesticides.